The proposed research has a goal of defining the relationship between chronic progressive renal disease and exposure to environmental hydrocarbon solvents. Clinial studies have established a relationship between human glomerulonephritis and hydrocarbon solvent exposure, in addition to the well known acute renal tubular toxicity of many of these agents. This study will attempt to produce an animal model of hydrocarbon-induced glomerulonephritis in rats by chronic intraperitoneal administration of common petroleum distillates and hydrocarbon solvents. Gasoline, carbon tetrachloride and toluene will be studied regarding their glomerulotoxic and nephrotoxic potential. The mechanism of induced injury will be studied by examining tissue with light, immunofluorescence and electron microscopy. If immunologic mechanisms are involved in perpetuating glomerulonephritis, this would explain why many cases of human glomerulonephritis are apparently mediated by immune mechanisms, but the antigens stimulating the immune response are unknown. N,N'-diacetylbenzidine has been shown to produce a proliferative glomerulonephritis in rats. We propose to study the pathogenesis of this glomerulonephritis which is morphologically similar to some forms of human glomerular disease. The role of the immune system in potentiating this toxin-induced glomerulonephritis and the exact location of glomerular and tubular cell injury will be studied by light, immunofluorescence and electron microscopy of renal tissue.